MECHANISMS OF SKELETAL MUSCLE FATIGUE
Principal Investigator: Jay Williams
Abstract: DESCRIPTION (Adapted from the applicant's abstract): Acute skeletal muscle activity often leads to the development of fatigue. The effects of fatigue are most often seen in venues such as the athletic arena, work site and rehabilitation clinic. In most instances, skeletal muscle fatigue results in decreased athletic performance and work productivity. However, in a number of cases, fatigue can increase ones susceptibility to orthopedic and musculo-tendinous injury and may lead to the development of muscle soreness. Although these consequences and the personal and financial costs of fatigue are well known, the mechanisms meditating this phenomenon are not completely understood. If means are to developed to prevent and alleviate both fatigue and its end results, then it is imperative that the fatigue process be fully understood. The overall objective of the proposed research is to gain insight into the mechanisms which mediate skeletal muscle fatigue. Fatigue appears to result from alterations in the excitation -contraction coupling process secondary to changes in the functional properties of the sarcoplasmic reticulum and the contractile apparatus or in the communication between the transverse tubule and SR. For years, it has been known that the onset of fatigue is associated with a reduction in the level of muscle glycogen and an accumulation of lactate. In addition, other glycolytic metabolites are elevated within the muscle fiber. This suggests that some aspect of carbohydrate metabolism influences skeletal muscle force output, possibly the depletion of glycogen or the accumulation of metabolites. Accordingly, the specific aims of this proposal are as follows. First, to determine if glycogen metabolites alter CA and SR function as well as TT-SR communication. Second, to determine if glycogen extraction, in vitro, alters CA and SR function as well as TT-SR communication. Third, to determine if glycogen depletion in skeletal muscle, in vivo, alters CA and SR function as well as TT-SR communication. The results of the proposed experiments will provide much needed information regarding the mechanisms which mediate skeletal muscle fatigue. In addition, it will attempt to identify direct links between muscle glycogen levels, CHO metabolism and the fatigue process.
Funding Period: 1994-03-01 - 2004-07-31
more information: NIH RePORT